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Volume 26, Issue 2, October 2015

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Mediterr J Rheumatol 2015; 26(2): 62-75
Symmetric and asymmetric dimethylarginines as biochemical markers of endothelial dysfunction and atherosclerosis in Rheumatoid Arthritis
Authors Information
1: Department of Rheumatology, Russels Hall Hospital, DudleyNHS FT, , United Kingdom
2: 4th Department of Internal Medicine, Ippokrateion Hospital, Thessaloniki, Greece
3: School of Sport, Health and Exercise Sciences, Bangor University, Gwynedd, Wales, United Kingdom
4: Arthritis Research UK Epidemiology Unit, University of Manchester, Manchester, United Kingdom
Abstract
Rheumatoid arthritis (RA) is associated with reduced life expectancy due to excess cardiovascular (CV) disease. Endothelial dysfunction is common in patients with RA, and accelerated coronary and cerebrovascular atherosclerosis are the major contributors to higher rates of CV events in RA compared to the general population. Nitric oxide (NO) produced by L-arginine is an important vasoactive agent for the maintenance of vascular health. The derangement of the NO/L-arginine pathway leads to vascular changes, predisposing to atherosclerosis. Nitric oxide metabolism is disrupted in RA, with a growing body of evidence suggesting that circulating inhibitors of NO synthase play a crucial role. Asymmetric (ADMA) and symmetric (SDMA) dimethylarginines have been recognized as emerging novel markers of endothelial dysfunction and CV morbidity and mortality in several CV disease settings; for example, coronary artery disease, stroke, lipids disorders, etc., as well as in the general population. Thus, it not surprising that they have been evaluated as indicators of vascular disease in RA. This paper provides an overview of the potential role and utility of these molecules in the pathophysiology of CV disease and the evaluation of endothelial function with a specific focus on RA patients.